RESUMEN
In a murine model (LCΔMHC-II) designed to abolish MHC-II expression in Langerhans cells (LCs), â¼18% of oral LCs retain MHC-II, yet oral mucosal CD4 T cells numbers are unaffected. In LCΔMHC-II mice, we now show that oral intraepithelial conventional CD8αß T cell numbers expand 30-fold. Antibody-mediated ablation of CD4 T cells in wild-type mice also resulted in CD8αß T cell expansion in the oral mucosa. Therefore, we hypothesize that MHC class II molecules uniquely expressed on Langerhans cells mediate the suppression of intraepithelial resident-memory CD8 T cell numbers via a CD4 T cell-dependent mechanism. The expanded oral CD8 T cells co-expressed CD69 and CD103 and the majority produced IL-17A [CD8 T cytotoxic (Tc)17 cells] with a minority expressing IFN-γ (Tc1 cells). These oral CD8 T cells showed broad T cell receptor Vß gene usage indicating responsiveness to diverse oral antigens. Generally supporting Tc17 cells, transforming growth factor-ß1 (TGF-ß1) increased 4-fold in the oral mucosa. Surprisingly, blocking TGF-ß1 signaling with the TGF-R1 kinase inhibitor, LY364947, did not reduce Tc17 or Tc1 numbers. Nonetheless, LY364947 increased γδ T cell numbers and decreased CD49a expression on Tc1 cells. Although IL-17A-expressing γδ T cells were reduced by 30%, LCΔMHC-II mice displayed greater resistance to Candida albicans in early stages of oral infection. These findings suggest that modulating MHC-II expression in oral LC may be an effective strategy against fungal infections at mucosal surfaces counteracted by IL-17A-dependent mechanisms.
RESUMEN
Dental implant diseases, peri-implantitis (PI) and peri-implant mucositis (PIM), have shown wide prevalence in recent studies. Despite the prevalence, diagnosing peri-implant disease (PID) remains challenging as common diagnostic methods of periodontal probing and radiographs may be inaccurate. These methods only document pre-existing destruction rather than current disease activity. Furthermore, there is no current model to predict the progression of PID. Though a predictive model is lacking, biomarkers may offer some potential. Biomarkers are commonly used in medicine to objectively determine disease state, or responses to a therapeutic intervention. Gingival crevicular fluid (GCF) biomarkers have moderate diagnostic validity in periodontitis. Biomarkers in peri-implant crevicular fluid (PICF) also show promising results in regard to their diagnostic and prognostic value. The aim of this review is to summarize the current knowledge of PICF biomarkers in the diagnosis of PID and evaluate their validity to predict disease progression. This review found that PICF studies utilize different methods of sampling and interpretation with varying validity (sensitivity and specificity). A number of promising diagnostic techniques were identified. Commercially available chair-side tests for MMP-8 to diagnose periodontal disease and PID activity are now available. Future directions include proteomics and metabolomics for accurate, site-specific diagnosis and prediction of PID progression. Although more research is needed, this review concludes that the assessment of proinflammatory cytokines (IL-1ß, TNFα, MMP-8) in the PICF may be of value to diagnose PI and PIM but current research remains insufficient to indicate whether biomarkers predict peri-implant disease progression.
RESUMEN
Mycosis fungoides (MF) is a cutaneous T-cell lymphoma that uncommonly involves the oral mucosa. Oral MF is an indication of systemic progression and is often associated with an unfavorable outcome. Any oral mucosal site may be affected. This report describes a case of MF involving the hard palate of a 64-year-old woman with confirmed skin MF. The histology showed intra- and subepithelial atypical lymphocytes. Immunohistochemistry on the tissue sections showed that the CD4:CD8 ratio was high (5.8:1) and the CD8:CD3 ratio was low (0.16:1). FoxP3(+) (forkhead box P3-positive) regulatory T cells were conspicuous within the infiltrate, but few interleukin-17 cells were observed. This report is the first to describe a detailed immune profile in oral MF.
